Heretofore, it has been known to treat Parkinson's disease with combination therapy utilizing L-DOPA and carbidopa. Parkinson's disease is believed to be a result of cholinergic overactivity due to a major derangement of the metabolism of dopamine and its synthesizing enzymes in the corpus striatum. Administration of dopamine, alone, is not an effective therapy since dopamine does not cross the blood brain barrier. L-DOPA, on the other hand, does cross the blood brain barrier where it is presumably converted to dopamine in the basal ganglia. However, only a small percentage of orally administered L-DOPA actually crosses the blood brain barrier due to the peripheral conversion of L-DOPA to dopamine by L-amino acid decarboxylase. Further, administration of L-DOPA is almost always associated with untoward side effects such as nausea, vomiting, hypotension, abnormal movements, and behavioral changes. In order for sufficient amounts of L-DOPA to cross the blood brain barrier, large doses of L-DOPA are required. Large doses of L-DOPA exacerbate these untoward side effects. In an attempt to overcome these problems, carbidopa is administered simultaneously with L-DOPA to inhibit peripheral decarboxylation of L-DOPA to dopamine, thus allowing greater quantities of a lower dose of L-DOPA to cross the blood brain barrier. Unfortunately, co-administration of L-DOPA plus carbidopa results in the same side effects as when L-DOPA is administered alone, only to a lesser extent.